IL-12 plays a pathologic role at the inflammatory loci in the development of diabetes in NOD mice

J Autoimmun. 2001 Mar;16(2):97-104. doi: 10.1006/jaut.2000.0469.

Abstract

Accumulating evidence suggests that CD4(+)T helper type 1 (Th1) cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse model. Interleukin (IL)-12 is a potent immunoregulatory molecule that is a key determinant of T-cell differentiation into Th1 cells, and has been implicated in the development of IDDM. To investigate the role of IL-12 that is locally produced by islet-infiltrating cells in the development of IDDM, we generated transgenic NOD mice in which the IL-12 p40 homodimer, a natural antagonist of IL-12, was produced exclusively in islets without affecting the levels of IL-12 p40 in the systemic circulation. We found that the incidence of diabetes was significantly reduced in these transgenic mice. These results clearly demonstrate that IL-12 locally produced by islet-infiltrating cells plays a critical role in the development of IDDM.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cyclophosphamide / pharmacology
  • Diabetes Mellitus, Type 1 / immunology
  • Diabetes Mellitus, Type 1 / pathology*
  • Dimerization
  • Female
  • Gene Expression
  • Glucagon
  • Immunosuppressive Agents / pharmacology
  • Incidence
  • Interleukin-12 / blood
  • Interleukin-12 / genetics
  • Interleukin-12 / immunology*
  • Islets of Langerhans / metabolism
  • Mice
  • Mice, Inbred NOD
  • Mice, Transgenic
  • Promoter Regions, Genetic

Substances

  • Immunosuppressive Agents
  • Interleukin-12
  • Cyclophosphamide
  • Glucagon